THE PATHOGENESIS of pancreatitis is not clearly defined. Intrapancreatic conversion of trypsinogen to trypsin is the most important, if not the sole, cause of this catastrophic illness.1-3 Therapeutic limitation and a high case fatality rate warrant our revaluation of experimentally induced pancreatitis, as modified by a trypsin inhibitor, in an effort to establish its possible specificity in the management of pancreatitis in humans.
The first objective was the confirmatory reproduction of acute pancreatitis through three successive events, creating intrapancreatic proteolytic trypsin activity1,2: (1) Entry of pancreatic secretion into the biliary tree by mixture of 1.35 gm of ox blood extract (Bilein) with 160,000 units of trypsin crystallized (Tryptar) (saline added); (2) Simulation of stasis in biliary system by incubation of mixture at 37 C (98.6 F) for 24 hr; and (3) Infusion of obstructed pancreatic duct with incubated material (20 cc) at low pressure (40 cm).
McHardy G, Craighead CC, Balart L, Cradic H, LaGrange C. Pancreatitis—Intrapancreatic Proteolytic Trypsin Activity: Evaluation of a Trypsin Inhibitor. JAMA. 1963;183(7):527–529. doi:10.1001/jama.1963.63700070001009
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